BCR-ABL binds to IRS-1 and IRS-1 phosphorylation is inhibited by imatinib in K562 cells
- Traina, Fabı́ola
- Carvalheira, José Barreto C
- Saad, Mario J.A
- Costa, Fernando F
- Saad, Sara T.O
Publication date
January 2003
DOI Publisher
Federation of European Biochemical Societies. Published by Elsevier B.V.Abstract
AbstractIn the present study we used K562 cells to demonstrate that insulin receptor substrate 1 (IRS-1) is expressed and constitutively phosphorylated in BCR-ABL+ cells. We observed association between BCR-ABL/IRS-1, IRS-1/phosphoinositide 3′-kinase (PI3-kinase), and IRS-1/Grb2 in the K562 cell line. Our findings demonstrate that imatinib treatment resulted in marked attenuation of BCR-ABL/IRS-1 association and of IRS-1-stimulated PI3-kinase activity in K562 cells. We concluded that the IRS-1 protein is involved in the signalling pathway of the BCR-ABL tyrosine kinase
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